The strongest mechanistic synthesis is membrane-associated organelle fission, with a single existing mitochondrial-fission core PMID:16172208(https://pubmed.ncbi.nlm.nih.gov/16172208/). The source-specific fusion and localization limits are retained in the annotation reasons and selected evidence.
GST-fold similarity is not sufficient to choose a native catalytic function. Positive engineered conjugation and ligand-binding findings remain visible alongside their construct and assay limits PMID:27841286(https://pubmed.ncbi.nlm.nih.gov/27841286/), PMID:42520938(https://pubmed.ncbi.nlm.nih.gov/42520938/). Natural product 2 is sequence-supported; the HuRI identifier is not proof of an isoform-specific physiological role PMID:15489334(https://pubmed.ncbi.nlm.nih.gov/15489334/), PMID:32296183(https://pubmed.ncbi.nlm.nih.gov/32296183/).
Neuropathy genetics supplies disease context without converting every clinical consequence into GDAP1's direct work. Detailed source access and preservation records are kept in the companion evidence files.
Partner-class binding capacity and native encounter are separate questions. The positive screen pairs remain, with explicit membrane-access limits for CLPP and compartment limits for selected other partners. The selected source evidence now supplies compact curated or primary anchors; primary TAGLN2 and BOK studies replace the earlier partner-GO rationale without assigning their activities to GDAP1.
The mitochondrial-fission core now uses only the mitochondrial outer membrane. Positive peroxisomal and liposome-deformation evidence remains in the membrane source discussion, with unresolved wild-type construct identity and translation-mixture limits. Three broad location terms are refined to established compartments. Native catalytic chemistry and endogenous ligand identity remain a biological question, distinct from those source-access limits.
Partner-class source attribution is explicit in the excerpt ledger: curated evidence arrays, absent per-field grades and selected primary-paper readings remain distinct. Those grades do not establish physiological contact with GDAP1.
Cellular peroxisomal-fission evidence is positive PMID:23628762(https://pubmed.ncbi.nlm.nih.gov/23628762/). The provenance discussion supersedes the earlier combined caveat: translation mixture limits the separate membrane-bending experiment, while the new human-annotation decision remains deferred.